The ileal crypt ultrastructural changes accompanying cryptosporidiosis in type 1 diabetic mouse model versus dexamethasone-immunocompromised mouse model.

Q3 Immunology and Microbiology
Journal of Parasitic Diseases Pub Date : 2025-09-01 Epub Date: 2025-02-25 DOI:10.1007/s12639-025-01789-0
Mennat-Elrahman A Fahmy, Amany A Abdel-Aal, Soad I Hassan, Maisa A Shalaby, Marwa Esmat
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Abstract

Cryptosporidiosis is an enteric infection caused by Cryptosporidium spp. The severity of the disease depends mainly on the immune status of the host. The infection is self-limited in immunocompetent individuals but in immunocompromised patients, it can be severe and threatening. To provide new insights into a better understanding of the pathogenesis of the infection and the impact of immune modulation on the course of the disease, we used 4 groups of Swiss-Albino mice; dexamethasone (DEX) group, the diabetic group, the DEX-infected group, and the diabetic-infected group. The blood glucose levels, oocyst shedding, mortality rates, and ultrastructural changes among study groups were observed and documented. The diabetic groups showed hyperglycemia while the DEX-infected group showed significantly higher oocyst shedding rates compared to the diabetic-infected group (P > 0.005). At the end of the experiment, the DEX groups showed higher mortality rates. Regarding the ultrastructural ileal crypt changes recorded in all groups, the DEX-infected group showed the severest changes with significantly lower numbers of Paneth cells, depletion of Paneth cell granules, and increased number of apoptotic crypt bodies significantly (P > 0.005) compared to the diabetic-infected group. On the contrary, the diabetic-infected group showed a significant expansion of Paneth cells with an increased number of granules and a significantly decreased number of apoptotic crypt bodies (P > 0.005). However, both models failed to control the infection properly highlighting the importance of early diagnosis and treatment of suspected immunocompromised cases.

1型糖尿病小鼠模型与地塞米松免疫功能低下小鼠模型隐孢子虫病伴回肠隐窝超微结构变化
隐孢子虫病是由隐孢子虫引起的一种肠道感染,其严重程度主要取决于宿主的免疫状态。这种感染在免疫功能正常的个体中是自限性的,但在免疫功能低下的患者中,它可能是严重和具有威胁性的。为了更好地了解感染的发病机制和免疫调节对疾病进程的影响,我们使用了4组瑞士白化小鼠;地塞米松组、糖尿病组、地塞米松感染组、糖尿病感染组。观察并记录各组的血糖水平、卵囊脱落、死亡率和超微结构变化。糖尿病组出现高血糖,dex感染组卵囊脱落率明显高于糖尿病感染组(P > 0.005)。在实验结束时,DEX组的死亡率更高。各组回肠隐窝超微结构变化中,dex感染组变化最严重,Paneth细胞数量明显减少,Paneth细胞颗粒消耗,凋亡隐窝小体数量明显增加(P > 0.005)。相反,糖尿病感染组Paneth细胞明显扩增,颗粒数量增加,凋亡隐窝体数量明显减少(P > 0.005)。然而,这两种模型都不能很好地控制感染,这突出了早期诊断和治疗疑似免疫功能低下病例的重要性。
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来源期刊
Journal of Parasitic Diseases
Journal of Parasitic Diseases Immunology and Microbiology-Parasitology
CiteScore
2.60
自引率
0.00%
发文量
86
期刊介绍: The primary constituency of the Journal of Parasitic Diseases is parasitology. It publishes original research papers (pure, applied and clinical), which contribute significantly to any area of parasitology. Research papers on various aspects of cellular and molecular parasitology are welcome.
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